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首页> 外文期刊>Psychopharmacology >Stress, sex hormones, inflammation, and major depressive disorder: Extending Social Signal Transduction Theory of Depression to account for sex differences in mood disorders
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Stress, sex hormones, inflammation, and major depressive disorder: Extending Social Signal Transduction Theory of Depression to account for sex differences in mood disorders

机译:压力,性激素,炎症和主要抑郁症:延长社会信号转导理论的抑郁症,以解释情绪障碍的性别差异

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Social Signal Transduction Theory of Depression is a biologically plausible, multi-level theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental adversity with internal biological processes that drive depression pathogenesis, maintenance, and recurrence. Central to this theory is the hypothesis that interpersonal stressors involving social threat (e.g., social conflict, evaluation, rejection, isolation, and exclusion) upregulate inflammatory processes that can induce several depressive symptoms, including sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. The original article describing this formulation (Psychol Bull 140:774-815, 2014) addressed critical questions involving depression onset and recurrence, as well as why depression is strongly predicted by early life stress and comorbid with anxiety disorders and certain physical disease conditions, such as asthma, rheumatoid arthritis, chronic pain, and cardiovascular disease. Here, we extend the theory to help explain sex differences in depression prevalence, which is a defining feature of this disorder. Central to this extension is research demonstrating that ovarian hormone fluctuationsmodulate women's susceptibility to stress, brain structure and function, and inflammatory activity and reactivity. These effects are evident at multiple levels and are highly context-dependent, varying as a function of several factors including sex, age, reproductive state, endogenous versus exogenous hormones, and hormone administration mode and dose. Together, these effects help explain why women are at greater risk for developing inflammation-related depressed mood and other neuropsychiatric, neurodevelopmental, and neurodegenerative disorders during the reproductive years, especially for those already at heightened risk for depression or in the midst of a hormonal transition period.
机译:抑郁症的社会信号转导理论是一种生物学卓越的多层次理论,描述了与内部生物过程中的社会环境逆变的经验联系起来的神经,生理学,分子和基因组机制。核心归属化理论是假设涉及社会威胁的人际关系压力源(例如,社会冲突,评估,拒绝,分离,排斥)上调炎症过程,可以诱导几种抑郁症状,包括悲伤情绪,厌氧,疲劳,精神术延迟,以及社会行为撤回。描述此配方的原始文章(Psychol Buarl 140:774-815,2014)涉及涉及抑郁发作和复发的关键问题,以及为什么抑郁受早期生命压力和焦虑症和某些物理疾病条件的抑郁症,以及某些物理疾病条件作为哮喘,类风湿性关节炎,慢性疼痛和心血管疾病。在这里,我们扩展了理论,以帮助解释抑郁症的性别差异,这是这种疾病的定义特征。该延伸的核心是研究表明,卵巢激素波动调节妇女对应力,脑结构和功能以及炎症活动和反应性的敏感性。这些效果在多个水平中是显而易见的,并且是高度上下文相关的,随着若干因素而变化,包括性别,年龄,生殖状态,内源性与外源激素和激素给药模式和剂量。这些效果在一起有助于解释为什么女性在繁殖年度发育炎症相关的抑郁情绪和其他神经精神,神经精神发育和神经变性疾病的风险更大,特别是对于已经提高了抑郁症风险的人或在激素过渡期间的那些时期。

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